Clostridium difficile infection (CDI) is one of the most common healthcare-associated infections (HAI) worldwide, causing substantial morbidity and mortality (Bartlett and Gerding, Clinical Infectious Diseases 2008, 46 Suppl 1, S12-8; Freeman et al., Clinical Microbiology Reviews 2010, 23, 529-49). C. difficile produces hardy spores, which are shed abundantly from the stool of patients with CDI, with contamination of patient skin, fomites, environmental surfaces, and hands of healthcare personnel (McFarland et al., The New England Journal of Medicine 1989, 320, 204-10; Bobulsky et al., Clinical Infectious Diseases 2008, 46, 447-50; Sethi et al., Infection Control and Hospital Epidemiology 2010, 31, 21-7). Patients acquire CDI by ingesting these ubiquitous spores, which germinate and proliferate in the intestine of individuals whose normal intestinal microbiota has been disrupted by exposure to antibiotics or proton pump inhibitors, or by weakened immunity (Bartlett and Gerding, Clinical Infectious Diseases 2008, 46 Suppl 1, S12-8; Freeman et al., Clinical Microbiology Reviews 2010, 23, 529-49; Cohen et al., Infection Control and Hospital Epidemiology 2010, 31, 431-55; Seekatz et al., The Journal of Clinical Investigation 2014, 124(10):4182-9; Britton and Young, Gastroenterology 2014, 146, 1547-53; Loo et al., The New England Journal of Medicine 2011, 365, 1693-703; Dubberke, Journal of Hospital Medicine 2012, 7 Suppl 3, S1-4; Chitnis et al., JAMA Internal Medicine 2013, 173, 1359-67; Dial et al., JAMA 2005, 294, 2989-95; Kwok et al., The American Journal of Gastroenterology 2012, 107, 1011-9). These vegetative C. difficile organisms elaborate exotoxins, with mucosal inflammation and injury, release of inflammatory mediators, and neutrophil recruitment (Britton and Young, Gastroenterology 2014, 146, 1547-53; Dupuy et al., Molecular Microbiology 1998, 27, 107-20; Kuehne et al., Nature 2010, 467, 711-3; Lyras, D.; O'Connor, J. R.; Howarth, P. M.; Sambol, S. P.; Carter et al., Nature 2009, 458, 1176-9). This toxin-mediated mucosal injury and host inflammatory response manifest clinically as pseudomembranous colitis with diarrhea, often accompanied by abdominal pain, fever, and leukocytosis, but may also result in a more fulminant clinical course with toxic megacolon, bowel perforation, septic shock, and death (Bartlett and Gerding, Clinical Infectious Diseases 2008, 46 Suppl 1, S12-8; Bartlett et al., The Journal of Infectious Diseases 1977, 136, 7015; Bartlett et al., The New England Journal of Medicine 1978, 298, 531-4). The attributable mortality of CDI is 5-10%, or approximately 14,000-20,000 deaths per year in the United States alone, making it one of the top 20 causes of death in individuals 65 years or older (Dubberke, Journal of Hospital Medicine 2012, 7 Suppl 3, S1-4; Dubberke et al., Infection Control and Hospital Epidemiology 2014, 35, 628-45; Hensgens et al., Clinical Infectious Diseases 2013, 56, 1108-16; Mitchell and Gardner, Antimicrobial Resistance and Infection Control 2012, 1, 20).